The natural intervertebral disc contains a jelly-like nucleus pulposus surrounded by a fibrous annulus fibrosus. Under an axial load, the nucleus pulposus compresses and radially transfers that load to the annulus fibrosus. The laminated nature of the annulus fibrosus provides it with a high tensile strength and so allows it to expand radially in response to this transferred load.
In a healthy intervertebral disc, cells within the nucleus pulposus produce an extracellular matrix (ECM) containing a high percentage of proteoglycans. These proteoglycans contain sulfated functional groups that retain water, thereby providing the nucleus pulposus within its cushioning qualities. These nucleus pulposus cells may also secrete small amounts of cytokines such as interleukin-1β and TNF-α as well as matrix metalloproteinases (“MMPs”). These cytokines and MMPs help regulate the metabolism of the nucleus pulposus cells.
In some instances of disc degeneration disease (DDD), gradual degeneration of the intervetebral disc is caused by mechanical instabilities in other portions of the spine. In these instances, increased loads and pressures on the nucleus pulposus cause the cells within the disc (or invading macrophases) to emit larger than normal amounts of the above-mentioned cytokines. In other instances of DDD, genetic factors or apoptosis can also cause the cells within the nucleus pulposus to emit toxic amounts of these cytokines and MMPs. In some instances, the pumping action of the disc may malfunction (due to, for example, a decrease in the proteoglycan concentration within the nucleus pulposus), thereby retarding the flow of nutrients into the disc as well as the flow of waste products out of the disc. This reduced capacity to eliminate waste may result in the accumulation of high levels of toxins that may cause nerve irritation and pain.
As DDD progresses, toxic levels of the cytokines and MMPs present in the nucleus pulposus begin to degrade the extracellular matrix, in particular, the MMPs (as mediated by the cytokines) begin cleaving the water-retaining portions of the proteoglycans, thereby reducing its water-retaining capabilities. This degradation leads to a less flexible nucleus pulposus, and so changes the loading pattern within the disc, thereby possibly causing delamination of the annulus fibrosus. These changes cause more mechanical instability, thereby causing the cells to emit even more cytokines, thereby upregulating MMPs. As this destructive cascade continues and DDD further progresses, the disc begins to bulge (“a herniated disc”), and then ultimately ruptures, causing the nucleus pulposus to contact the spinal cord and produce pain.
One proposed method of managing these problems is to remove the problematic disc and replace it with a porous device that restores disc height and allows for bone growth therethrough for the fusion of the adjacent vertebrae. These devices are commonly called “fusion devices”, or “interbody fusion devices”.
Current spinal fusion procedures include approaches such as transforaminal lumbar interbody fusion (TLIF), posterior lumbar interbody fusion (PLIF), and extreme lateral interbody fusion (XLIF). TLIF and PLIF spinal fusion surgeries require refraction of neural tissues including the spinal cord and/or exiting nerve roots. Retraction is typically performed with hand held dural retractors that are manually placed and secured by an operative assistant who is standing on the contralateral side of the patient.
This position across from the surgeon greatly reduces visibility of the neural retraction for the operative assistant, increasing the risk of neural damage. Frequent adjustment of the retractor is required to ensure proper positioning, distance and the amount of dural retraction force applied. Significant patient risk, including dural tears, can be incurred if excessive retraction is applied or if the spinal cord is inadvertently released during the procedure.
In addition, the presence of the neural retractor crowds or obscures the surgical site, thereby minimizing visibility and access to the disc space for the operating surgeon.
Cloward, “A Self-Retaining Spinal Dural Retractor” J Neurosurg., 1952 March; 9(2):230-2, discloses a modified Hoen laminectomy retractor having a retraction spatula.
U.S. Pat. No. 7,569,054 (Michelson) discloses a tubular member having a passage and opposing bone penetrating extensions adapted to piece opposed vertebral bodies.
The objective of this device is to reduce operative site crowding to enhance disc access while providing for consistent and stable dural retraction.